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OCT. 16-18,

Carbon Monoxide Poisoning In
Children: Diagnosis And Management
In The Emergency Department
Approximately 5000 children present annually to emergency departments in the United States with unintentional carbon monoxide poisoning. Children may be more vulnerable to carbon monoxide poisoning because of their increased metabolic demand and their inability to
vocalize symptoms or recognize a dangerous exposure. Developing
fetuses and newborn infants are more vulnerable to carbon monoxide
poisoning because of the persistence of fetal hemoglobin. Mild carbon
monoxide poisoning may present as viral symptoms in the absence
of fever. While headache, nausea, and vomiting are the most common presenting symptoms in children, the most common symptom in
infants is consciousness disturbance. This review discusses the limitations of routine pulse oximetry and carboxyhemoglobin measurement in determining carbon monoxide exposure, and notes effects of
co-ingestions and comorbidities. Although the mainstay of treatment
is 100% oxygen, the current evidence and controversies in the use of
hyperbaric oxygen therapy in pediatric patients are reviewed, along
with its possible benefit in preventing delayed neurologic sequelae.
Adam E. Vella, MD, FAAP
Associate Professor of Emergency
Medicine, Pediatrics, and Medical
Education, Director Of Pediatric
Emergency Medicine, Icahn School
of Medicine at Mount Sinai, New
York, NY

Associate Editor-in-Chief
Vincent J. Wang, MD, MHA
Professor of Pediatrics, Keck
School of Medicine of USC;
Associate Division Head, Division
of Emergency Medicine, Children's
Hospital Los Angeles, Los Angeles,

Editorial Board
Jeffrey R. Avner, MD, FAAP
Professor of Pediatrics and Chief
of Pediatric Emergency Medicine,
Albert Einstein College of Medicine,
Children’s Hospital at Montefiore,
Bronx, NY
Steven Bin, MD
Associate Clinical Professor
of Emergency Medicine and
Pediatrics, UCSF School of
Medicine; Medical Director, UCSF
Benioff Children's Hospital, San
Francisco, CA
Richard M. Cantor, MD, FAAP,
Professor of Emergency Medicine
and Pediatrics, Director, Pediatric
Emergency Department, Medical
Director, Central New York Poison
Control Center, Golisano Children's
Hospital, Syracuse, NY

September 2016
Volume 13, Number 9

Theodore E. Macnow, MD
Assistant Professor of Pediatrics, University of Massachusetts
Medical School; Pediatric Emergency Medicine Division, UMass
Memorial Medical Center, Worcester, MA
Mark L. Waltzman, MD, FAAP
Chief of Pediatrics, South Shore Hospital; Assistant Professor
of Pediatrics, Harvard Medical School; Division of Emergency
Medicine, Boston Children’s Hospital, Boston, MA
Peer Reviewers
Michael Levine, MD
Assistant Professor, Department of Emergency Medicine,
Division of Medical Toxicology, University of Southern California,
Los Angeles, CA
Nima Majlesi, DO, FAAEM
Director of Toxicology, Staten Island University Hospital;
Assistant Professor of Emergency Medicine, SUNY Downstate,
New York, NY
Prior to beginning this activity, see “Physician CME Information”
on the back page.

Ilene Claudius, MD
Associate Professor of Emergency
Medicine, Keck School of Medicine
of USC, Los Angeles, CA

Alson S. Inaba, MD, FAAP
Garth Meckler, MD, MSHS
Pediatric Emergency Medicine
Associate Professor of Pediatrics,
Specialist, Kapiolani Medical Center
University of British Columbia;
for Women & Children; Associate
Division Head, Pediatric Emergency
Professor of Pediatrics, University
Medicine, BC Children's Hospital,
Ari Cohen, MD
of Hawaii John A. Burns School of
Vancouver, BC, Canada
Chief of Pediatric Emergency Medicine
Services, Massachusetts General
Joshua Nagler, MD, MHPEd
Hospital; Instructor in Pediatrics,
Madeline Matar Joseph, MD, FACEP, Assistant Professor of Pediatrics,
Harvard Medical School, Boston, MA

Harvard Medical School; Fellowship
Director, Division of Emergency
Marianne Gausche-Hill, MD, FACEP, Professor of Emergency Medicine
Medicine, Boston Children’s
Director, Pediatric Emergency
Hospital, Boston, MA
Medical Director, Los Angeles
Medicine Division, University
County EMS Agency; Professor of
James Naprawa, MD
MedicineClinical Medicine and Pediatrics,
Attending Physician, Emergency
Jacksonville, Jacksonville, FL
David Geffen School of Medicine at
Department USCF Benioff
UCLA, Los Angeles, CA
Michael J. Gerardi, MD, FAAP,
FACEP, President
Associate Professor of Emergency
Medicine, Icahn School of Medicine
at Mount Sinai; Director, Pediatric
Emergency Medicine, Goryeb
Children's Hospital, Morristown
Medical Center, Morristown, NJ

Stephanie Kennebeck, MD
Associate Professor, University of
Cincinnati Department of Pediatrics,
Cincinnati, OH
Anupam Kharbanda, MD, MS
Chief, Critical Care Services
Children's Hospitals and Clinics of
Minnesota, Minneapolis, MN

Tommy Y. Kim, MD, FAAP, FACEP
Sandip Godambe, MD, PhD
Associate Professor, Loma Linda
Vice President, Quality & Patient
University Medical Center and
Safety, Professor of Pediatrics and
Children's Hospital, Department of
Emergency Medicine, Attending
Emergency Medicine, Division of
Physician, Children's Hospital of the
Pediatric Emergency Medicine, Loma
King's Daughters Health System,
Linda, CA
Norfolk, VA
Melissa Langhan, MD, MHS
Ran D. Goldman, MD
Associate Professor of Pediatrics and
Professor, Department of Pediatrics,
Emergency Medicine; Fellowship
University of British Columbia;
Director, Director of Education,
Co-Lead, Division of Translational
Pediatric Emergency Medicine, Yale
Therapeutics; Research Director,
University School of Medicine, New
Pediatric Emergency Medicine, BC
Haven, CT
Children's Hospital, Vancouver, BC, Robert Luten, MD
Professor, Pediatrics and
Emergency Medicine, University of
Florida, Jacksonville, FL

Children's Hospital, Oakland, CA
Joshua Rocker, MD
Assistant Chief of Emergency
Medicine and Pediatric, Hofstra
School of Medicine; Associate
Director, Division of Pediatric
Emergency Medicine, Cohen
Children's Medical Center, New
Hyde Park, NY
Steven Rogers, MD
Associate Professor, University of
Connecticut School of Medicine,
Attending Emergency Medicine
Physician, Connecticut Children's
Medical Center, Hartford, CT

David M. Walker, MD, FACEP, FAAP
Director, Pediatric Emergency
Medicine; Associate Director,
Department of Emergency Medicine,
New York-Presbyterian/Queens,
Flushing, NY

International Editor
Lara Zibners, MD, FAAP, FACEP
Honorary Consultant, Paediatric
Emergency Medicine St. Mary's
Hospital Imperial College Trust,
London, UK; Nonclinical Instructor
Emergency Medicine Icahn school
of medicine at Mount Sinai, New
York, NY

Pharmacology Editor
James Damilini, PharmD, MS, BCPS
Clinical Pharmacy Specialist,
Emergency Medicine, St. Joseph's
Hospital and Medical Center,
Phoenix, AZ

Quality Editor
Steven Choi, MD
Assistant Vice President, Montefiore
Network Performance Improvement;
Director, Montefiore Institute for
Performance Improvement; Assistant
Professor of Pediatrics, Albert
Einstein College of Medicine, Bronx,

Christopher Strother, MD
Assistant Professor, Emergency
Medicine, Pediatrics, and Medical
CME Editor
Education; Director, Undergraduate
Deborah R. Liu, MD
and Emergency Department
Assistant Professor of Pediatrics,
Simulation; Icahn School of Medicine
Keck School of Medicine of USC;
at Mount Sinai, New York, NY
Division of Emergency Medicine,
Children's Hospital Los Angeles,
Los Angeles, CA

Case Presentations

plex. The girl was found in her bed by the fire department.
According to the rescuer, the room was hot with smoking
carpet and filled with thick smoke. In the ambulance, the
girl was minimally responsive to painful stimuli. Her vital
signs were remarkable for tachycardia, with a heart rate
around 130 beats/min, but were otherwise stable. In the
ED, her heart rate remains 130 beats/min, her blood pressure
is now 68/36 mm Hg, her respiratory rate is 24 breaths/
min, and her oxygen saturation is 100% on 15 L/min by
nonrebreather mask with an oxygen reservoir. The girl has a
GCS score of 8, with eye opening only to painful stimuli and
nonlocalization of pain. Her speech is not comprehensible.
There are soot debris and superficial burns to her face and
neck, with a demarcation line representing the blanket. She
has a normal cardiorespiratory and abdominal examination.
The patient is intubated with a 5.0 cuffed endotracheal tube.
Soot was noted in the larynx. She is ventilated at 24 breaths/
min with 100% oxygen and given 40 mL/kg of lactated
Ringer’s solution with an improvement in her blood pressure to 100/62 mm Hg. The venous blood gas results show
a mixed metabolic and respiratory acidosis and her lactate
result is 12.4 mmol/L. Her COHb level is 18%. Her cyanide
level is pending. As you begin to think about the next
steps, you wonder: How should comorbid CO and cyanide
poisoning be treated? Given that the patient has burns, CO
poisoning, and suspected cyanide poisoning with critical
care needs, can she possibly still be a candidate for hyperbaric
oxygen therapy? What can you advise her parents about her
prognosis and potential complications?

You receive notification that EMS is bringing in a
14-year-old hockey goalie after a syncopal event. EMS
inform you that he is the first of many potential victims
en route after multiple players and spectators at a local ice
rink began complaining of different symptoms. According
to EMS, a noninvasive pulse CO-oximeter reported his
COHb level at 21%. His GCS score was 14 at the scene
due to confusion and disorientation, his vital signs were
stable, and he was given oxygen by nonrebreather face
mask. His blood glucose was 115 mg/dL. On arrival, the
patient’s vital signs are normal with an oxygen saturation of 100% on 15 L/min of oxygen by nonrebreather
face mask. The goalie complains of severe 9/10 frontal
headache, nausea, and ringing in his ears. On physical
examination, his face is flushed, and he is diaphoretic with
an otherwise normal physical examination and mental
status. His CBC, electrolytes, and arterial blood gas
analysis are in the normal range. His COHb level is 19%.
His ECG is normal. As you prepare to manage the patient
and other potential victims, you ask yourself: What was
the source of this poisoning and are others in danger?
What are the most common symptoms of carbon monoxide poisoning in children? What are the treatment goals?
What are the indications for consulting with a hyperbaric
medicine specialist?

A 2-month-old girl is brought to the ED by her mother
with a chief complaint of “lethargy.” The baby was in her
usual state of health until this morning when she had to
be aroused by her mother. The infant fed poorly, having
a weak latch and feeding for only 5 minutes. The mother
notes that she herself has been feeling nauseous and has a
mild headache, and wonders if the baby caught her “virus.”
On examination, the infant’s vital signs are: temperature,
36.9°C (98.4°F); heart rate, 155 beats/min; blood pressure,
76/42 mm Hg; respiratory rate, 46 breaths/min; oxygen
saturation, 99% on room air. The baby is lethargic on
examination, arousing and crying for IV placement, but
then quickly falling asleep again. She has a normal cardiorespiratory and abdominal examination. Grasping reflex
is not present bilaterally and moro reflex is diminished.
She has diminished truncal tone but intact reflexes. You
consider the broad differential for the lethargic-appearing
infant: Sepsis? Nonaccidental trauma? Cardiac arrhythmia? Adrenal insufficiency? The patient is started on 5
L/min of oxygen by face mask. Her blood glucose is 80
mg/dL. She is given a 20 mL/kg bolus of normal saline
and antibiotics. A head CT shows normal anatomy with
no acute bleeding or infarction. Her ECG is normal for
her age. The COHb returns with the blood gas at 28%.
You ask yourself: What are the next steps in treatment
of CO poisoning in an infant? Can a baby be referred for
hyperbaric oxygen therapy? Who should be called regarding home safety concerns? What was the source of the CO
and who else is at risk? Should the mother be treated?

A 6-year-old girl is brought to the ED by EMS after
being rescued from a 3-alarm fire at an apartment comCopyright © 2016 EB Medicine. All rights reserved.

Carbon monoxide (CO) has been called a “silent
killer.” It is formed by the incomplete combustion of
hydrocarbon fuels and, as it is both clear and odorless, is undetectable by the human senses. It rapidly
diffuses into the pulmonary circulation and competes with oxygen to bind the hemoglobin molecule,
thereby impairing oxygen delivery.

The toxic effects of CO poisoning have been
known for centuries. As early as the 4th century BC,
Aristotle cautioned that coal fumes lead to a “heavy
head” and death.1 Until the mid 20th century, coal
was the primary heating fuel in the urban United
States, and accidental CO-related fatalities from
improper ventilation or heater malfunction were not
uncommon.2 With cleaner-burning fossil fuels, more
efficient engines, and advances in energy technology,
CO levels in the air and rates of CO poisoning have
fallen. In 1923, Henderson and Haggard measured
CO from a moving car in New York City and found
levels in city traffic to range from 10 to 290 parts per
million (ppm); today, air levels are generally less
than 1 ppm.3

Despite a historical decline, CO remains one of
the leading causes of poisoning-related emergency
department (ED) visits, with 50,000 cases annually
in the United States.4-7 CO poisoning is responsible


for 500 unintentional, non–fire-related deaths annually in the United States, more than any other gas.4,8
The incidence of CO poisoning has a seasonal and
geographic association with cold climates, peaking during winter months and occurring at higher
rates in high-altitude states, notably the north and
Midwest.4,7,9 However, cases occur year-round, so
clinicians must remain suspicious for less-common
and evolving sources of exposure.10

The presentation of CO poisoning can range
from mild and nonspecific to critical illness, depending on the level and duration of the exposure and
host factors. Because symptoms can mimic a myriad
of conditions and a source of exposure is not always
known, the diagnosis may remain hidden if clinicians are not vigilant in maintaining an awareness
and suspicion for CO poisoning.

The mainstay for treatment of CO poisoning is
oxygen therapy. In severe cases, the emergency clinician must weigh the risks and benefits of transfer
to a center with capabilities for hyperbaric oxygen
(HBO) therapy, the evidence for which remains controversial.

In this issue of Pediatric Emergency Medicine Practice, the current state of diagnosis and management
of CO poisoning in children in the ED is reviewed.
The unique developmental and physiologic traits of
children with this condition will be considered. The
current epidemiology of CO poisoning is defined
and put it into a historical context to better understand how sources and prevention strategies for CO
poisoning have evolved over time. Current research
topics are explored, including noninvasive detection,
laboratory and radiographic markers for disease
severity, HBO therapy, and other therapies for the
treatment of CO poisoning.

Critical Appraisal Of The Literature
A PubMed search strategy, developed in consultation with a medical librarian, searched all Englishlanguage human studies related to CO published
from November 2009 through January 2015. A combination of the following search terms were used:
carbon monoxide poisoning, carbon monoxide, ACOP,
poison, toxicology, toxicity, poisoning, CO poisoning, CO
toxicity, human, humans, adult, infant, infancy, child,
pediatric, pediatrics, middle age, teen, adolescent, adolescents, adolescence, children, patient, patients, and age.
This strategy yielded 477 articles; 211 were relevant
to this review topic.

The review was then extended to include bibliographic references of relevant literature prior to the
queried date range including review articles that cite
studies dating back to 1950.11,12 Clinical guidelines
and policies from relevant professional organizations related to CO poisoning that were published
over the past 30 years were searched. The American
September 2016 •

College of Emergency Physicians (ACEP) published
an evidence-based Clinical Policy on critical issues
in the management of adult patients presenting to
the ED with acute CO poisoning.13 The Cochrane
Database of Systematic Reviews had a single review
that was most recently updated in 2011 related to
CO regarding the use of HBO.14

A targeted search on the use of HBO in children
was performed. A PubMed query with the terms
carbon monoxide and hyperbaric was performed for
English-language review articles and clinical trials
from January 1985 through February 2015. This strategy yielded 133 publications that were reviewed.
Limiting the search in PubMed to only pediatrics
yielded 17 results, of which there were several
review articles and case series on HBO therapy
use in pediatric CO poisoning, but no randomized
controlled trials or case-control studies. None of the
review articles cite any randomized controlled trials
of HBO use in pediatric CO poisoning.

Epidemiology And Etiology
Accidental, non–fire-related CO poisoning, sometimes called “preventable” or “unintentional” CO
poisoning, is responsible for approximately 20,000
ED visits and nearly 500 deaths annually in the United States.6,8 Unintentional CO poisoning in pediatric
patients represents about 5000 ED visits annually
in the United States. In a 2012 national surveillance
data analysis, children aged < 5 years had the highest estimated rate of accidental CO-related ED visits
(11.6 cases/100,000 population), followed by adults
aged 25 to 34 years (10.4 cases/100,000 population).
Despite having a higher rate of ED visits compared
to other age groups, rates of hospitalizations and
deaths from CO poisoning are lower in children.8

The United States Centers for Disease Control and
Prevention (CDC) data on unintentional, non–fire-related cases of CO poisoning from 1999 to 2004 show an
annual death rate of 1.53 cases/1 million citizens in the
United States.9 Overall, northern geography is associated with a higher rate of CO poisoning.4,8,9 The death
rate is highest in the Mountain States and High Plains
States as well as Alaska, which has an annual death
rate of 4.8 cases/1 million citizens.9 Wyoming has the
highest death rate with 6.2 cases/1 million; Hawaii’s
death rate was too low to calculate with accuracy.6
There are more CO poisoning-related deaths in the
winter months.9 On average, the death rate from CO
poisoning in the United States is about 2 persons daily
in December and January and 0.67 in July and August.9

CO is formed by the incomplete combustion of
hydrocarbons, which include many fuels used for
energy (eg, gasoline, wood, charcoal, propane, natural gas, oil, and kerosene). Common sources of CO
include poorly maintained or ventilated home-heating systems and cooking appliances, motor vehicle
3 Copyright © 2016 EB Medicine. All rights reserved.

exhaust, charcoal grills, space heaters, and portable
generators.10,15 Paint stripper (methylene chloride) is
quickly metabolized to CO in the liver, and exposure
to its fumes or its ingestion is a rare cause of CO poisoning. Exposures most often occur at home (73%).6

Ice resurfacers (ie, Zamboni machines) have
been reported to contribute to elevated CO levels in
indoor ice arenas.16-18 In December 2014, 92 people
presented to Wisconsin EDs with symptoms of CO
poisoning attributed to a propane-fueled ice resurfacer; 1 player and a pregnant spectator received
HBO treatment.19

In the United States, attempted suicide by CO
poisoning often occurs through exposure to motor
vehicle exhaust and cooking ovens. There are case
reports of suicide attempts from charcoal burning
in the United States, a practice that is endemic in
parts of Asia.20-22 Tobacco products, including hookah smoking, which has seen increased popularity
among adolescents and young adults in the United
States, can cause acute or chronic CO poisoning.23-30
There is an increase of CO poisoning during national
disasters resulting from damaged equipment and
the improper use of portable generators.31,32 After
blizzards, CO poisoning can result from snowblocked exhaust pipes of idling automobiles.

fects seen in CO poisoning are in CO binding other
intracellular molecules.39,40 In addition, 10% to 15%
of absorbed CO is bound to extracellular molecules.
In 1976, Goldbaum et al published a study comparing dogs that inhaled high concentrations of CO to
dogs that were infused with erythrocytes with 80%
COHb.39 All of the dogs that inhaled CO demonstrated toxic effects and died, despite having similar
COHb levels to the dogs that were infused with
COHb (all of which survived). This study implies
that the major contributor to toxicity is CO’s inhibition of other molecules, namely cytochrome oxidase,
which impairs mitochondrial respiration.

The half-life of CO bound to other intracellular and extracellular molecules may be longer
than COHb. These interactions may cause oxidative stress,41 impaired mitochondrial respiration
via inhibition of cytochrome oxidase,42 thrombus
formation,43,44 and inflammation,36 which, together
with CO’s negative effects on oxygen delivery, cause
synergistic cardiac and neurological damage.35,36,42
CO binds to platelet and endothelial heme proteins
such as nitric oxide synthase, which causes the
release of nitric oxide. Nitric oxide may contribute to
the hypotension seen in some CO-poisoned patients.
It produces peroxynitrite (a strong oxidant), which
contributes to oxidative stress and binds cytochrome
c, further inhibiting mitochondrial respiration.36,45
Tissue hypoxia and impaired cellular respiration
cause activation of stress responses and inflammation, leading to further apoptosis and necrosis similar to pathways seen in tissue reperfusion injury.36
Mitochondrial and myocardial dysfunction from CO
in the heart may cause ischemia and dysrhythmias,
even with adequate oxygen delivery.46,47

CO is of similar density to ambient air, so it diffuses
and lingers in an unventilated room and neither rises
to the ceiling nor falls to the floor. CO molecules are
small enough to penetrate through most drywall in
the United States.33 It rapidly diffuses into the pulmonary circulation and reversibly binds the heme
moiety of hemoglobin at 200 to 250 times the affinity
of oxygen, creating carboxyhemoglobin (COHb).34,35

At normal physiologic levels, endogenous CO
functions as a neurotransmitter and may favorably
modulate inflammation and the cell cycle.36 However,
at levels > 2% COHb, CO impairs the ability of heme
to deliver oxygen both by directly occupying oxygenbinding sites and by causing a conformational change
to the other 3 oxygen-binding sites. The conformational change in the other oxygen-binding sites increases their affinity for oxygen and decreases oxygen
off-loading in peripheral tissues. These effects shift
the oxygen-hemoglobin dissociation curve leftward
and make it more hyperbolic. (See Figure 1, page 5.)

The half-life of COHb is about 300 minutes; thus,
it begins to accumulate in the blood within a short
exposure time. With normobaric oxygen (NBO)
therapy (which is 100% inhaled oxygen at normal
atmospheric pressure), the half-life is decreased to
between 50 and 100 minutes; with HBO therapy, the
half-life can be reduced to 30 minutes.37,38

While COHb is easily measured and is a marker
for toxicity, the major contributor to the toxic efCopyright © 2016 EB Medicine. All rights reserved.

Pathophysiology In Children And Infants
Children have increased minute ventilation compared to adults, which should make them more vulnerable to accumulating CO. Symptoms in children
are difficult to assess retrospectively, and there is
conflicting evidence about whether young children
are more or less symptomatic at a given COHb level
compared to adults. Physiologically, children should
experience symptoms at a lower COHb level because of their increased metabolic rate and oxygen
demand, which has been demonstrated in some
case series.48-50 However, a retrospective review
of 261 children with CO poisoning found that the
severity and number of symptoms on presentation
for a given COHb level was higher in adolescents
compared to toddlers and infants.51 The argument of
younger children being more resilient to CO poisoning is also supported by epidemiologic evidence that
overall rates of hospitalizations and deaths are lower
in young children.8

Neonates may be more vulnerable to CO
poisoning because of the natural leftward shift of
the dissociation curve of fetal hemoglobin.47 Fetal


hemoglobin both accumulates and eliminates CO
more slowly than hemoglobin A.52 Young children
or children with special needs are more vulnerable
to CO poisoning from a developmental perspective,
as they may not be able to communicate symptoms,
have awareness of a dangerous situation, or be able
to move from a given location.

Prevention Of Carbon Monoxide Poisoning
Efforts in preventing accidental CO poisoning focus
on the use of alarm detection devices, public education, and legislation. Because CO is generated by
incomplete combustion, successful environmental
and public health efforts aimed at promoting cleaner
energy and decreasing air pollution have also
decreased the rates of CO poisoning.2 The United
States Occupational Safety and Health Administration defines the maximum occupational acceptable
level of CO as an 8-hour time-weighted average
of 50 ppm; however, the CDC National Institute
for Occupational Safety and Health recommends
an occupational 8-hour time-weighted average of
35 ppm.53 The World Health Organization (WHO)
recommends an indoor limit of 8.7 ppm of CO over
an 8-hour period for COHb to remain less than
2.5%, even when a normal person engages in light

Figure 1. The Effect Of
Carboxyhemoglobinemia On Oxygen
Content And Delivery

or moderate exercise.54 Similarly, the United States
Environmental Protection Agency recommends that
indoor air not exceed 9 ppm CO.45 Only Minnesota,
Massachusetts, and Rhode Island have regulations
in place regarding indoor ice rink air quality.55-57

There are no federal regulations mandating the
need for CO alarms in buildings; their use is regulated at the state and local levels. As of March 2016, 30
states had enacted statutes regarding the necessity of
CO alarms in buildings; however, there is variability in the applicability and strength of the laws.58,59
CO alarm limits are set by UL (formerly known as
Underwriters Laboratories) and are time-concentration dependent, in that they alarm within minutes
at a high level (ie, 400 ppm), but may take over an
hour to alarm at their lowest level (ie, 70 ppm).60
Prior to the late 1990s, alarm standards were lower,
but because of many false positives, UL thresholds
were increased.61 CO alarms only warn of imminent
danger and may not detect chronic CO exposure.
Lower-limit models are available commercially and
are usually owned by local fire departments.

A large proportion of adults in the United States
are unaware of the risks of operating fossil fuel-powered equipment indoors.62 Different localities have featured public service campaigns (with varied success)
regarding proper generator placement, maintenance of
fuel-burning appliances, idling automobiles, and the
use of CO detectors.63 Public service announcements,
sometimes multilingual, are often aired during times of
increased risk for CO poisoning (eg, disasters, snowstorms, and winter months).32,64 Public service announcements can be on television, radio, and Internet
social media. Following a record snowfall in Massachusetts in February 2013, public radio broadcasts,
Twitter®, and Internet blogs warned about the danger
of CO poisoning from idling a car before shoveling out
the exhaust pipe.65 The CDC website is a good source
for patient information on CO poisoning prevention
and symptoms (

Differential Diagnosis

Abbreviations: COHb, carboxyhemoglobin; O2Hb, oxyhemoglobin;
PO2, partial pressure of oxygen.
Reprinted from: Carbon Monoxide, Second Edition, International
Programme on Chemical Safety, World Health Organization,
Environmental Health Criteria, No. 213. Copyright 1999. With
permission from the World Health Organization. Available at: http://

September 2016 •

CO poisoning can be considered a “great mimic,”
as the constellation of symptoms is often nonspecific. Without a known source of exposure or clues
such as other sick contacts, the differential remains

The most common presenting symptoms in children are headache and nausea. Without an exposure
history, mild to moderate CO poisoning can be easily confused with a viral illness, food poisoning, or
other causes of headache. In a study of children presenting to the ED with afebrile viral symptoms who
were found on history to have a potential source of
CO exposure, 50% of the children had elevated (>
2%) COHb levels, while 13% of children had COHb
levels > 10%.49 In this series, all patients with COHb
5 Copyright © 2016 EB Medicine. All rights reserved.

The American Association of Poison Control
Centers (1-800-222-1222) should be contacted in all
cases of suspected CO poisoning. Poison control
centers are available to offer assistance in ED management as well as to coordinate and recommend
transfer to an HBO facility. Cases reported to local
poison control centers are reported to the American
Association for Poison Control Centers National
Poison Data System for epidemiologic tracking.

levels > 2% had symptomatic improvement with
oxygen administration, suggesting CO was responsible for their presenting symptoms.

More-severe poisoning may be confused with
other causes of altered mental status such as trauma,
diabetic ketoacidosis, meningitis, hypoglycemia,
and intoxications. Altered level of consciousness is
the most common symptom of severe CO poisoning
in younger children and infants.66 The differential
for an unwell-appearing infant is broad, including
trauma, congenital heart disease, sepsis, inborn error
of metabolism, or electrolyte abnormality. Chronic
CO poisoning is even more insidious and can mimic
depression, chronic fatigue syndrome, migraines,
and other chronic neurologic and psychiatric conditions.67

Initial Stabilization
Emergency evaluation of moderate to severe CO
poisoning should occur similarly to any other
critical patient requiring resuscitation. The patient
should be immediately placed on cardiopulmonary
monitoring. Initial attention should be given to the
primary survey: airway, breathing, and circulation.

Prehospital Care

Primary Survey
The patency of the patient's airway should be assessed with careful attention to inspection of the
face and oropharynx for burns, trauma, and carbonaceous material. If the airway is not patent, basic
airway maneuvers should be performed. Airway
management should occur per local protocols, with
maintenance of cervical spine precautions if concurrent trauma is suspected.

Respiratory effort should be assessed, with
inspection of the chest for movement and signs of
trauma. All lung fields should be auscultated for
air entry. Assisted breathing with a bag-valve mask
and 100% oxygen therapy should be initiated for
patients with inadequate respiratory effort. Passive 100% oxygen therapy with a face mask and
reservoir should be given to patients with adequate
respiration. Capnography can be helpful to monitor
and trend a child’s respiratory effort and end-tidal
carbon dioxide. Note that routine pulse oximetry is
spuriously elevated in CO poisoning and does not
accurately reflect a patient’s hypoxemia.

A thorough cardiovascular examination should
be performed and should focus on signs of contributing cardiogenic shock such as a bradycardia, an
irregular rate (dysrhythmia), muffled heart sounds
(tamponade), or an S3 sound (heart failure). Central
and peripheral pulses should be palpated. Fluid
resuscitation and vasoactive medications should
be given to patients with shock. Unilateral absent
peripheral pulses may indicate a limb-threatening
vascular injury or a compartment syndrome that can
result from rhabdomyolysis due to immobility and/
or the direct toxic effect of CO.70

First and foremost, emergency responders must ensure scene safety. This may include allowing the fire
department to remove a source of exposure, or at least
allowing measurement of air CO levels prior to approaching the patient. There are case reports of emergency medical service (EMS) personnel becoming
victims of CO poisoning themselves when responding to a call where the CO level was very high.68,69

The next priority is to remove the victim from
the source of exposure. Oxygen should be applied in
all cases of suspected CO poisoning. Because there
is a possibility of comorbidities or co-intoxicants
in CO-poisoned patients, EMS personnel should
perform a complete primary and secondary survey.
When possible, prehospital intravenous (IV) access
and electrocardiography (ECG) may be helpful, but
these measures should not delay oxygen therapy.

In circumstances where triaging is necessary,
infants, victims who are most symptomatic, pregnant women, and patients with very high levels on
noninvasive CO detection (if available) should be
prioritized for transport to the ED.

Emergency Department Evaluation
Because the acuity of a child with CO poisoning can
range from a complaint of mild symptoms (headache or “viral-like”) to severe (prearrival notification of a child en route who might be comatose or
in cardiopulmonary arrest), the approach in the ED
will be variable. Often the diagnosis of CO poisoning is based on a combination of having a known or
suspected exposure, consistent signs or symptoms,
and laboratory evaluation of COHb. On initial presentation, the differential should remain broad, and
emergency clinicians must remain suspicious for the
presence of comorbidities, co-intoxicants, or trauma
that may have led to the exposure or happened as a
result of the CO poisoning.
Copyright © 2016 EB Medicine. All rights reserved.

Patient Presentation
Symptoms of CO poisoning are nonspecific and
variable, the history often provides the most valuable clues to diagnosis. Each patient is unique in
his or her presentation at a certain COHb level.


Symptom severity is dependent on the acuity of the
exposure and host factors and is more pronounced
with exercise or other exertional activities because
of an increased demand for oxygen.19 CO poisoning
should be suspected in all fire victims and considered in children with known sources of exposure.

The most common symptoms of mild to moderate CO poisoning in adults and children are headache and nausea/vomiting.35,49,51 Other common
symptoms are dizziness, lightheadedness, confusion, fatigue, chest pain, and shortness of breath.71
Generally, it has been described that mild CO
intoxication (< 20% COHb) produces headache, mild
dyspnea, myalgias, visual changes, and confusion.
Moderate poisoning (20%-40% COHb) is associated
with drowsiness, lightheadedness, vomiting, dulled
sensation, dizziness, shortness of breath, and chest
pain. Severe poisoning (> 40% COHb) manifests as
weakness, lethargy, incoordination, and short-term
amnesia. There may be vital sign instability, and
cardiovascular and neurologic collapse is imminent. Above 60% COHb, patients may be comatose,
suffer convulsions, and die.35,36,72 Nonetheless, a
2012 review of 1323 patients referred for HBO in
the Undersea and Hyperbaric Medical Society/
CDC CO Poisoning Surveillance System found that
symptoms alone cannot be accurately correlated to a
given COHb level and that there is a large spectrum
of possible presenting symptoms.71 (See Table 1,
page 8.) Given the lack of specificity of symptoms,
both presentation and COHb level should be taken
into account when determining the severity of CO

Young children may lack the ability to explain
symptoms they are experiencing. While older children manifest symptoms similar to adults, symptoms in infants might be as vague as irritability and
poor feeding. In a case series of 30 children with
severe CO poisoning, disturbance of consciousness
was found to be the most common symptom in
young children and infants.66

Exposure History
Potential sources for CO exposure should be assessed in all children with nonspecific symptoms,
especially in the absence of fever. It is important to
ask about where and when symptoms began and
whether there is a pattern to the symptoms. For
example, did symptoms begin while in a motor vehicle? Are the symptoms present at home but not at
school? Or are the symptoms worse in the morning?
Practitioners might inquire whether a residence recently began using a combustible-fuel heating source
(ie, kerosene heater, wood stove, fireplace, natural
gas appliance, Sterno® unit, or central heating system). Close contacts who have symptoms or known
CO poisoning should cause a clinician to suspect a
common exposure. The sudden death or illness of
September 2016 •

household pets may be a harbinger for human CO
poisoning and provide a clue of gas exposure.73-75

Most exposures occur at home rather than at
work or school.3 In a prospective study of 483 patients, the most common time period for CO poisoning presenting as headache was between midnight
and 10:00 AM.76

Some helpful questions that might reveal a potential CO exposure include:
• Are there any pets at home? Are they acting
• Are other close contacts having similar or seemingly unrelated symptoms?
• Is there a daily pattern to the symptoms?
• Has the child had a fever? (Not usually present
with CO poisoning)
• Where was the child when the symptoms began?
• Have household heating equipment, generators,
or other appliances been recently turned on?
• Do you have a CO detector at home? When was
it last tested? (Ideally, once per month)
• When was the last time the household heating
system was inspected? (Ideally, annually)
• Was noninvasive CO-oximetry performed by
EMS in the field?

Physical Examination
A thorough and complete physical examination/
secondary survey is warranted in suspected CO poisoning and should focus on assessing for comorbid
conditions and signs of organ dysfunction. Special
attention should be given to the cardiopulmonary
and neurologic examination, which may help a
clinician decide on acute interventions and whether
transfer to an HBO center is warranted.

Although there is a trend for more-severe poisoning to be associated with vital sign abnormalities,
there are no abnormal vital sign patterns specific to
CO poisoning.77 A retrospective case series of 476 patients aged > 16 years with CO poisoning found that
68% of patients with COHb levels > 20% had normal
vital signs.77

A complete cardiopulmonary assessment should
be performed as described in the primary survey
and repeated with the secondary survey. CO can
have direct toxic effects on the heart, leading to dysrythmias78,79 and myocardial dysfunction.80,81 Serial
cardiovascular examinations should be performed
to assure adequate perfusion to peripheral tissues. A
careful respiratory examination in combination with
radiographic imaging helps find contributing factors
to respiratory insufficiency. Victims of smoke inhalation are at risk for pneumonitis or acute respiratory
distress syndrome. Trauma victims may have rib
fractures, pulmonary contusions, hemothoraces, or
pneumothoraces. Obtunded patients may have aspirated. Patients with asthma may have contributing
7 Copyright © 2016 EB Medicine. All rights reserved.

lower airway obstruction from other noxious gases.

Skin examination may reveal erythema; however, classic “cherry-red” skin and lips have been
found to be present in only a minority of CO intoxications and are not prognostically useful in assessing the severity of CO poisoning.82 Patients with
thermal injury may appear red, whereas those with
shock may be pale. Because of potentially prolonged
immobility and the direct toxic effects of CO on
muscles, patients with severe CO poisoning may
develop pressure ulcers and necrosis to the skin,
subcutaneous tissue, and muscle, especially at pressure points or body parts stuck under objects.

A detailed neurological examination including
mental status, coordination and gait, cranial nerves,

strength, sensation, and reflexes should be performed. A depressed Glasgow Coma Scale (GCS)
score is associated with more-severe CO poisoning.
A myriad of neurologic deficits from CO poisoning
have been reported in the literature, including ataxia,83 deafness,84 weakness,85 and a positive Babinski
reflex.86 Neurologic deficits may require additional
imaging to characterize their etiology and are associated with delayed neurologic sequelae.

Delayed Neurologic Sequelae
Delayed neurologic sequelae represent a broad spectrum of neurologic deficits, cognitive impairments,
affective disorders, and epilepsy that can persist for
weeks to months after CO poisoning; in some cases,
they are permanent. The pathophysiology is still uncertain, but likely is a result of many of the pathways
for injury. A randomized controlled trial comparing HBO to NBO therapy in adults with severe CO
poisoning found cognitive sequelae in 25% of HBOtreated patients at 6 weeks postexposure and 18% at
1 year compared to 46% of NBO-treated patients at
6 weeks and 33% at 1 year.8 Children seem to be less
vulnerable to delayed neurologic sequelae, with rates
ranging from 1% to 25% in different case series.87-89
It is difficult to ascertain the exact rate of delayed
neurologic sequelae from these case series because
they included a small number of patients and are
heterogeneous in their populations, treatments, and
definitions of delayed neurologic sequelae.

There are no clear predictors for delayed neurologic sequelae on presentation, although prolonged
or severe exposure and neurologic deficits (including altered mental status) have been linked to higher
rates of delayed neurologic sequelae.11,66,88 Currently, there is much research interest in imaging and
biomarkers that might predict delayed neurologic
sequelae shortly after an exposure. In adults, S-100b,
a calcium-binding protein produced by astroglia in
the brain and used as a marker of neuronal damage
after brain trauma, has shown promise in predicting
delayed neurologic sequelae; however, its use is not
routine at this time in most settings.90,91 Brain magnetic resonance imaging (MRI) may be useful for
predicting delayed neurologic sequelae in the subacute phase (days to weeks after the exposure) and
new diffusion-weighted and susceptibility-weighted
imaging techniques may improve their detection
ability.92,93 Classic findings on MRI scans of patients
with CO poisoning include symmetrically abnormal
globus pallidi, although there is a broad spectrum of
gray and white matter abnormalities reported, even
in siblings with the same exposure.94,95

Table 1. All Symptoms Reported By Patients
With Acute Carbon Monoxide Poisoning,
Grouped By Organ System
• Chest pain, heaviness,
fullness, tightness
• Left arm pain
• Palpitations
• Abdominal pain
• Diarrhea
• Fecal incontinence
• Hematemesis
• Nausea
• Vomiting
• Xerostomia
• Aphasia
• Confusion
• Coordination problems
• Dysarthria
• Facial droop
• Gait disturbance, ataxia,
balance problems
• Headache
• Hemiparesis
• “Jerky” movements
• Loss of consciousness
• Memory complaints
• Numbness (focal, diffuse)
• Pain (numerous sites)
• Paraparesis
• Paresthesias
• Seizure
• Tremor
• Twitching

• Ocular burning or pain
• Vision disturbance (blindness,
blurring, diplopia, scotomata)
• Dizziness
• Hearing loss
• Tinnitus
• Vertigo
• Anxiety
• Cough
• Dyspnea
• Flank pain
• Urinary incontinence
• Chilling
• Diaphoresis
• Drowsiness
• Fatigue
• Fussiness
• Giddiness
• Hot flashes
• Irritability
• Lethargy
• Lightheadedness
• Muscle cramps
• Myalgias
• Rash

Diagnostic Studies

Neil B. Hampson, Susan L. Dunn. Symptoms of carbon monoxide
poisoning do not correlate with the initial carboxyhemoglobin
level. Undersea & Hyperbaric Medicine. 2012;39(2):657665. http:// Reproduced with
permission from the Undersea and Hyperbaric Medical Society.

Copyright © 2016 EB Medicine. All rights reserved.

Arterial Blood Gas
Arterial blood gas (ABG) analysis in CO poisoning


often reveals a normal acid-base status and partial
pressure of oxygen, arterial (PaO2). The oxygen
saturation reading on blood gas analysis may be
spuriously normal, depending on the type of analyzer used by the laboratory. In cases of severe CO
poisoning, the ABG might reveal a metabolic lactic
acidosis.96 In fire victims, an ABG with severe
metabolic lactic acidosis (ie, pH < 7.20) should
prompt consideration of cyanide poisoning and
empiric treatment.40

Most institutional laboratories perform spectrophotometric methods to measure COHb. While COHb
levels should be obtained and trended, the clinical
picture should dictate treatment, as COHb levels
do not reflect the chronicity of the exposure nor the
amount of CO bound to other molecules. COHb
levels may confirm the diagnosis of CO poisoning
and be trended for improvement, but they are only a
surrogate measure of the morbidity of CO. Chronic
exposures may have a worse clinical presentation
at a given COHb level than acute exposures, due to
cumulative effects of hypoxemia and the accumulation of CO bound to cellular molecules other than
hemoglobin. In addition, the COHb measured in the
hospital will be influenced by any oxygen treatment
administered in the field.

Venous COHb levels have been found to be as
accurate as arterial COHb;97 however, ABG is often
preferred in a clinical situation with a critically ill
patient to assess for acid-base status and PaO2, which
will often be normal in CO poisoning. Noninvasive
COHb detection is now available for bedside detection of CO poisoning. (See the “Controversies And
Cutting Edge” section, page 15.)

Smokers can have a chronically elevated COHb,
normally between 3% and 5%, though the level may
be up to 10% or higher.24,40,98,99 The reported normal
range of COHb in nonsmokers is < 3%; however,
evidence supports that “normal” might be as low
as 1% to 2%, and a level of 3% indicates a potential
exposure.36,49,99 A study of 200 preoperative patients
found that passive (second-hand) smoking was not
associated with elevations of COHb in children.100
This finding is supported by a larger cross-sectional
study in adults that did not find a clinically significant difference in COHb levels between adults
exposed and not exposed to household smoking.101

There is a wide overlap between COHb blood
levels and clinical symptoms.71 Classically, in adults,
symptoms begin at a COHb level of approximately
10%. In children, symptoms have been reported with
COHb levels as low as 3%; the symptoms subsequently improve with oxygen therapy.49

Complete Blood Count
A complete blood count should be obtained to
screen for anemia, which should be corrected in
September 2016 •

cases of CO poisoning to maximize the oxygen-carrying capacity of the blood.

Blood urea nitrogen and creatinine will provide information on baseline renal function and can be trended
to screen for acute kidney injury. An assessment of
acid-base, glucose, and electrolyte status will also be
obtained from this laboratory assessment.
Creatine Kinase
In a patient with altered mental status who may have
been unconscious or trapped for a long period of time,
creatine kinase may help quantify suspected muscle
breakdown. Myoglobin deposition in renal tubular
cells may precipitate acute kidney injury.
Cyanide testing is not useful acutely because of a lag
time in obtaining the result, though it might be sent
to later confirm an exposure. If cyanide poisoning is
suspected, patients should be empirically treated.
A point-of-care glucose test should be obtained in all
patients with altered mental status. Hypoglycemia is
correctable and may contribute to impaired cellular
Lactate has been found to be an independent predictor for CO poisoning severity in adults and may be
a better marker for tissue hypoxia and end-organ
damage than PaO2.96,102 In adults, lactate levels
strongly correlate with elevated COHb and troponin.96 Elevated lactate levels (> 2 mmol/L) are predictive of the need for admission as well as a higher
likelihood of serious medical complications during
a CO poisoning admission.96,102 Elevated lactate in
a fire victim without significantly elevated COHb
levels may indicate cyanide toxicity.

Pregnancy Test
In females of reproductive age, a urine or serum
human chorionic gonadotropin level is necessary to
screen for pregnancy. Should an adolescent with CO
poisoning be pregnant, it is important to consult obstetrics for a fetal assessment. Fetal hemoglobin has
a delayed and prolonged absorption of CO, and the
fetus may have worse distress than the mother.52,103
Emergent cesarean delivery for fetal distress or HBO
therapy may be indicated in these patients depending upon the gestational age. (See the “Special Circumstances: Pregnancy” section, page 14.)

Urine toxicology, ethanol, acetaminophen, and salicylate
levels should be considered in adolescent patients with
9 Copyright © 2016 EB Medicine. All rights reserved.

Clinical Pathway For The Diagnosis And Management Of
Carbon Monoxide Poisoning In Pediatric Patients
Patient presenting to ED with:
• Viral symptoms in the absence of
• Neurologic symptoms
• Altered mental status
• Headache
• Chest pain
• Shortness of breath
• A possible source of CO exposure

• Apply 100% oxygen by NRB mask
(Class I)
• Consider noninvasive CO-oximetry, if
available (Class II)
• Obtain COHb level

COHb ≤ 2%

Consider other etiologies

Consider discharge
if home safety allows


COHb between 2% and 10%

COHb ≥ 10%

• Continue 100% oxygen by NRB
mask (Class I)
• Obtain CBC, chemistries, fingerstick
glucose, lactate, blood gas, and
pregnancy test (if indicated)
• Consider ECG and troponin if
symptoms of cardiac dysfunction are
• Consider CXR and head CT as
clinically warranted
• Place on bed rest, minimize anxiety
• Recheck COHb in 2 hours

• Continue 100% oxygen by NRB
mask (Class I)
• Obtain CBC, chemistries, fingerstick
glucose, lactate, blood gas, and
pregnancy test (if indicated), ECG,
• Consider CXR and head CT as
clinically warranted
• Place on bed rest, minimize anxiety
• Recheck COHb in 2 hours
• Correct anemia < 10 g/dL (Class III)
• Maintain urine output > 1 mL/kg/h
if myoglobinemia or myoglobinuria
(Class I)
• Obtain early consultation with HBO
specialist (Class III)

Is COHb now ≤ 2% and have
symptoms resolved?

• Admit for continued oxygen therapy
• Consider transport to HBO facility
(Class III)

Admit for continued oxygen therapy

Abbreviations: CBC, complete blood count; COHb, carboxyhemoglobin; CT, computed tomography; CXR, chest x-ray; ECG, electrocardiogram; HBO,
hyperbaric oxygen; NRB, nonrebreather.
See page 11 for Class of Evidence definitions.

Copyright © 2016 EB Medicine. All rights reserved.



suspected CO poisoning. These examinations can help
narrow the differential diagnosis of a patient presenting
with altered mental status and can help explain altered
mental status, vital sign abnormalities, or other symptoms not entirely explained by CO poisoning alone. It is
possible that intoxication may have led to the event that
caused the CO exposure, or that the patient is presenting
with a polysubstance suicide attempt. In a retrospective
study of 426 patients with intentional CO poisoning, cointoxicants were found in 42% of patients.104

(palpitations, chest pain, shortness of breath, hypotension), altered mental status, or severe CO poisoning.


Computed Tomography

A urinalysis is useful to screen for myoglobinuria or
microscopic evidence of acute kidney injury.

A head computed tomography (CT) scan should
be performed on suspected trauma patients with
altered mental status and should be considered in
nontrauma patients with a depressed GCS score
and/or neurologic deficits on examination. Because
the mainstay of therapy for CO poisoning is oxygen,
often treatment can be administered while obtaining a CT, which is useful for ruling out intracranial
abnormalities that could contribute to the patient’s
symptoms. Head CTs are not useful in the acute
setting for diagnosing or prognosticating delayed
neurologic sequelae.

ECGs should be considered in all pediatric patients
with suspected CO poisoning who exhibit signs or
symptoms of cardiac dysfunction, have a depressed
mental status, suffer from a predisposing condition,
or have severe CO poisoning. ECG analysis may
show cardiac ischemia, dysrhythmias, or evidence
for co-ingestants.

Cardiac Markers (Creatine Kinase-MB Or
Troponin T)
Myocardial ischemia has been reported in one-third of
adults with moderate to severe CO poisoning.105 While
both ischemic ECG changes and troponin are sensitive for myocardial injury in adults with CO poisoning,105,106 in children, troponin may be more sensitive
for cardiac injury.106 A retrospective review of 107
pediatric patients with CO poisoning found that 15%
of children presenting with COHb > 10% had elevated
troponins, and all of the children had normal ECGs.
Fifty percent of the children with elevated troponins
had abnormal echocardiograms demonstrating decreased ejection fractions and depressed left ventricular
function that resolved by hospital discharge.107

Cardiac enzymes should be considered in pediatric patients with an underlying cardiac condition,
those with signs or symptoms of cardiac dysfunction

Chest Radiography
A chest x-ray should be obtained in patients with hypoxemia, respiratory signs or symptoms, or predisposing conditions. A chest x-ray can help guide the
emergency clinician to appropriately treat confounding respiratory insufficiency, thus maximizing a
patient’s ability to oxygenate at a given COHb level.

Cardiopulmonary resuscitation should be performed
as required. The goals of treating CO poisoning
specifically are to (1) maximize oxygen delivery and
(2) decrease oxygen consumption until the CO has
been eliminated through the pulmonary circulation.
Oxygen is the mainstay for CO therapy and should
be administered through a nonrebreather mask with
a reservoir so that inspired air is 100% oxygen. If a
patient requires intubation, he should be ventilated
with 100% oxygen. Oxygen therapy should be continued until the COHb level is < 3% and the patient
is asymptomatic. To optimize the blood’s oxygencarrying capacity, clinicians should have a low
threshold for correcting anemia in severe CO poisoning.72 To decrease oxygen consumption, patients

Class Of Evidence Definitions
Each action in the clinical pathways section of Pediatric Emergency Medicine Practice receives a score based on the following definitions.
Class I
• Always acceptable, safe
• Definitely useful
• Proven in both efficacy and effectiveness

Level of Evidence:
• One or more large prospective studies
are present (with rare exceptions)
• High-quality meta-analyses
• Study results consistently positive and

Class II
• Safe, acceptable
• Probably useful

Level of Evidence:
• Generally higher levels of evidence
• Nonrandomized or retrospective studies:
historic, cohort, or case control studies
• Less robust randomized controlled trials
• Results consistently positive

Class III
• May be acceptable
• Possibly useful
• Considered optional or alternative treatments

Level of Evidence:
• Generally lower or intermediate levels of
• Case series, animal studies,
consensus panels
• Occasionally positive results

• Continuing area of research
• No recommendations until further

Level of Evidence:
• Evidence not available
• Higher studies in progress
• Results inconsistent, contradictory
• Results not compelling

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright © 2016 EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Medicine.

September 2016 •

11 Copyright © 2016 EB Medicine. All rights reserved.

should be placed on bed rest and anxiety-provoking
activities should be avoided as much as possible.
This may be accomplished by allowing a child to sit
with his or her parent, dimming the lights, utilizing
child life specialists when available, and minimizing
noncritical medical interventions. Anxiolytics should
be avoided in patients with altered mental status.

It is important to recognize and treat other
contributing causes to cardiorespiratory insufficiency beyond the CO itself. This may include
interventions such as giving bronchodilators to
a patient with asthma, pain control to a trauma
victim, vasopressors to a hypotensive patient, or
noninvasive respiratory support to a hypopneic
infant. Fire victims may need treatment for cyanide poisoning with hydroxocobalamin or sodium
thiosulfate without nitrite-containing compounds.
(See the “Special Circumstances: Fire Victims” section, page 15.)

In patients with evidence of rhabdomyolysis,
urine output should be maintained at > 1 mL/
kg/h to protect the kidneys from injury. In patients
with normal baseline renal function, this might be
accomplished with IV hydration and/or diuretics
(furosemide 0.5-1 mg/kg IV or mannitol 0.25-1 g/
kg IV) if necessary.72 A urinary catheter may be
necessary to monitor hourly urine output.

ber. (See Figure 2.) There are over 200 hyperbaric
facilities in the United States that treat approximately
1500 patients with CO poisoning annually.108 There
are no set protocols for HBO treatment of CO poisoning. Depending on the treatment center, a "dive"
may last between 30 and 120 minutes, be at different
pressures, and be repeated for a variable number of

HBO therapy increases hydrostatic pressure and
tissue oxygen tension, which hastens the clearance of
CO from hemoglobin (reducing the half-life of COHb
to about 30 minutes) and shifts the hemoglobindissociation curve to the right.37,38 By eliminating
COHb, HBO therapy may be beneficial in decreasing
acute morbidity and mortality. However, it is likely
that the possible benefit of HBO in reducing delayed
neurologic sequelae is through accelerated elimination of CO from cytochrome oxidase, preventing lipid
peroxidation and oxidative brain injury, even in the
presence of normalized COHb levels.87

The role of HBO therapy in CO poisoning remains controversial. There are 5 published randomized controlled trials and an abstract of a randomized
controlled trial interim analysis with a total of 1361
participants comparing HBO to NBO.11,109-113 Four trials showed no benefit and 2 found HBO therapy to be
highly effective in the reduction of neurologic sequelae.
There is heterogeneity in the clinical and statistical
methodology of these trials. A Cochrane review that
was updated in 2011 and included the 6 CO poisoning
trials above concluded that, “HBO cannot be routinely
recommended for the treatment of CO poisoning.
It is possible that some patients, particularly those

Hyperbaric Oxygen Therapy
HBO therapy is defined as administration of oxygen
at > 1 atmosphere of absolute pressure. This is accomplished by placing the patient in a hyperbaric cham-

Figure 2. A Multiplace Hyperbaric Oxygen Chamber

Image used with permission from OxyHeal Health Group, Inc.

Copyright © 2016 EB Medicine. All rights reserved.



with more severe poisoning may derive benefit, but
this remains unproven.”14 The ACEP Clinical Policy
reached similar level C recommendations that, “1.
HBO is a therapeutic option for CO-poisoned patients;
however, its use cannot be mandated. 2. No clinical
variables, including COHb levels, identify a subgroup
of CO-poisoned patients for whom HBO is most likely
to provide benefit or cause harm.”13

Some of the trials included in the Cochrane
review included pediatric patients of varying ages
while others were limited to adults. In our literature
search, there were no randomized controlled trials or
published subanalyses looking at the benefit of HBO
in children. The study by Waisman et al is the largest
study of HBO use in children and it retrospectively
examined 139 patients, including 111 children treated
for CO poisoning.89 There was 1 death and no side
effects from HBO therapy reported in this group. A
retrospective review of 14 infants (aged < 2 years) also
found no side effects attributable to HBO, though 1
infant died of anoxic brain injury.114

There is some evidence that HBO therapy
might be beneficial in preventing delayed neurologic sequelae in children; however, no randomized controlled trials have been published and no
formal recommendations exist. The 1987 retrospective analysis by Kim and Coe found lower rates of
delayed neurologic sequelae in 56 children treated
with HBO compared to 51 treated with NBO (29% vs
19%).88 Waisman et al reported delayed neurologic
sequelae in 2 of 111 children treated with HBO for
CO poisoning, fewer than in most other cases series
of CO poisoning in children.89

There is no widespread agreement on the indications for HBO therapy in adults or children. Table 2
demonstrates generally accepted criteria as well as indications for consideration of HBO therapy in children.

COHb levels above 20% to 25% in children or
above 15% in pregnant women are often included
as criteria for HBO referral; however, a COHb level
below these values should not rule out an HBO referral. COHb level is dependent on the time elapsed
and oxygen therapy delivered since the exposure,
and does not reflect CO bound to other molecules.
Therefore, persistence of symptoms is an indication
for referral, even with mildly elevated COHb levels.

There are physiologic and practical considerations in treating pediatric patients with HBO.88 (See
Table 3.) Middle ear and sinus barotrauma are more
common in children compared to adults receiving
HBO due to their smaller anatomy and increased
frequency of otitis and upper respiratory infections
in this population. Myringotomy is often indicated
in young children who cannot perform the necessary maneuvers to equalize middle ear pressure,
older children with active otitis media, or comatose
patients. Because one of the goals of therapy is to
minimize oxygen demand, hyperbaric chambers
September 2016 •

that allow nonstatic toys or parents to accompany
the child and those that are equipped with television
may help to minimize a child’s anxiety. It is possible
that pediatric-trained personnel or equipment may
need to accompany the child to an HBO facility to
assist in the management of the patient. Neonates

Table 2. Indications For Hyperbaric Oxygen
Therapy After Carbon Monoxide Poisoning
Generally Accepted Criteria
• Syncope
• Severe neurologic symptoms on presentation (seizures, focal
neurologic findings, coma)
• Myocardial ischemia diagnosed by history or electrocardiography
• Cardiac dysrhythmias (ventricular, life-threatening)
• Persistent neurologic symptoms and signs after several hours
of 100% oxygen therapy at ambient pressure (mental confusion,
visual disturbance, ataxia)
• Pregnancy (symptomatic, carboxyhemoglobin level > 15%,
evidence of fetal distress)
Criteria for Consideration
• Carboxyhemoglobin level > 20% to 25%
• Abnormal results on neuropsychological examination
• Age < 6 months with symptoms (lethargy, irritability, poor feeding)
involved in the same exposure as adults with any of the above
• Children who have underlying disease (ie, sickle cell anemia) for
whom hypoxia may have deleterious effects
Reprinted from: Erica Liebelt. Hyperbaric oxygen therapy in childhood
carbon monoxide poisoning. Current Opinion in Pediatrics.
1999;11(3):259-264. With permission from Wolters Kluwer Health.

Table 3. Practical Considerations For The
Pediatric Hyperbaric Patient
• Pediatric equipment for the hyperbaric chamber
• Pediatric doses of commonly administered medications
immediately available
• Physicians and support personnel trained in pediatric
resuscitations and sedation
• Monoplace versus multiplace chambers
• Distraction techniques (ie, televisions, video cassette recorders,
non–static-producing toys and games)
• Parental presence and support
• Instruction of children in ways to maintain Eustachian tube function
(yawning, chewing, Frenzel or Valsalva maneuvers)
• Myringotomies for comatose, intubated children and selected
infants and children unable to cooperate with maneuvers
• External heating devices, such as warming blankets and waterfilled devices, to maintain temperature
• Neonatal and infant conditions

Oxygen toxicity to the retina


Congenital lung malformations


Uncorrected or unpalliated ductal-dependent congenital heart

Reprinted from: Erica Liebelt. Hyperbaric oxygen therapy in childhood
carbon monoxide poisoning. Current Opinion in Pediatrics.
1999;11(3):259-264. With permission from Wolters Kluwer Health.

13 Copyright © 2016 EB Medicine. All rights reserved.

may be at a higher risk of retinopathy of prematurity
from HBO therapy. Chest x-rays may be performed
on neonates to look for undiagnosed lung conditions
vulnerable to rupture and pneumothorax.

Risks and benefits should be weighed carefully,
and consultation with a neonatologist is warranted.
Oxygen is a stimulus for ductus arteriosus closure, so
infants may require echocardiographic examination
if there is concern for an underlying congenital heart
defect. A chest x-ray might be considered to rule out
underlying congenital lung pathology at risk for a
pneumothorax. Hyperoxia is known to cause retinopathy of prematurity in preterm infants, and the effect
of HBO therapy on the preterm and term infant is not
fully elucidated.89,115 Ophthalmologic examination
should be performed following HBO treatments in
premature infants. These concerns should not prevent
emergency clinicians from providing NBO as soon as
the diagnosis of CO poisoning is suspected.

Generally, patients may be safely discharged from the
hospital when they are asymptomatic and their COHb
level is < 5%. Emergency clinicians should assure that
patients have a safe place to go and that they do not to
return to the site of the exposure until the source has
been identified and it has been deemed safe by the fire
department. Patients with persistent symptoms, higher
COHb levels, evidence of end-organ dysfunction, or
other medical or social concerns may require inpatient
hospitalization or HBO therapy referral. If there are
home safety or neglect concerns, appropriate consultations to child protection or social services may delay
discharge from the ED or warrant inpatient admission.
Patients suspected of intentional CO poisoning need
evaluation by a mental health professional and likely
inpatient psychiatric admission.

It is important to consider both the mother and the
unborn fetus. As with neonates, fetuses may be
more vulnerable to CO poisoning because of their
increased metabolic demand and fetal hemoglobin. CO passes through the placenta both by passive diffusion and facilitated transport. During an
exposure, the fetus is initially hypoxemic purely due
to a decrease in maternal oxygen; later, fetal COHb
develops as CO begins to dissociate from maternal
hemoglobin and cross the placenta, reaching maximal fetal concentrations after about 4 hours.119 Fetal
COHb levels are approximately 10% to 15% higher
than maternal levels and elimination is slower.120

In cases of severe poisoning, it may be necessary
to consult an obstetrician to perform a fetal assessment or emergent cesarean delivery. Pregnant patients
should be treated immediately with NBO, and it may
be necessary to treat them for 5 times the duration that
it takes the mother’s COHb level to be < 5%.119

Though generally thought to be safe and efficacious, there are no formal recommendations or
randomized controlled trials regarding the use of
HBO therapy in pregnancy. Pregnant patients were
excluded from all randomized controlled trials in
the Cochrane review. Although there are different
cut-offs, most recommendations for HBO include
pregnancy with a COHb level of 15%, which is
lower than for other adults.121 A prospective study
of fetal outcomes in CO poisoning found no physical or neurobehavioral deficits in 31 infants whose
mothers had mild to moderate CO poisoning, and in
cases of severe CO poisoning, there were no adverse
outcomes in the 2 fetuses treated with HBO, while 3
of the 5 treated with NBO had adverse outcomes.122
In another prospective series of 44 pregnant women
with CO poisoning referred for HBO, 2 had spontaneous abortions, neither of which was felt to be related to HBO.123 A 25-year single-center study from
France found no differences in height and weight or
6-year health and development assessments between
children treated with HBO for CO poisoning in utero
and matched controls.124

Special Populations And Circumstances
Newborns may be especially vulnerable to CO poisoning due to their high metabolic rate and persistence of fetal hemoglobin.50 The immature central
nervous system of neonates is more vulnerable to
CO-induced hypoxia and lipid peroxidation.115
Fetal hemoglobin can persist until 6 months of life,
and at 21 days of life, still represents about 70% of
circulating hemoglobin.116 Fetal hemoglobin has a
natural left shift compared to adult hemoglobin A
and it accumulates and eliminates CO more slowly.52
Fetal hemoglobin may spuriously elevate laboratory
COHb readings, especially in older-model CO-oximeters.117 Newer-model laboratory CO-oximeters that
use multiple wavelengths of light are less susceptible to this artifact.118 The diagnosis of CO poisoning, especially in the absence of other sick contacts,
is difficult, because infants cannot describe their
symptoms. The most common presenting symptom
is consciousness disturbance, which can range from
fussiness to lethargy. The differential for unwell-appearing infants is broad, including infection, metabolic disorders, cardiac disease, and nonaccidental
trauma. Other etiologies should be explored simultaneously while obtaining COHb levels and starting oxygen therapy. Emergency clinicians must be
careful to prevent hypoglycemia and hypothermia,
which can be seen in critically ill infants.

Premature newborns have additional risks with
oxygen therapy that are not seen in other populations,
and there is a paucity of experience with HBO therapy
in preterm infants and neonates in the literature.87,115
Copyright © 2016 EB Medicine. All rights reserved.



Fire Victims

Chronic Carbon Monoxide Exposure

Victims of fires are at risk for thermal and chemical
airway injury, cyanide poisoning, methemoglobinemia, carbon dioxide asphyxiation, and other
complications of smoke inhalation. Smoke is a
heterogeneous mixture of toxins, chemical fumes,
asphyxiants, and particulate debris, each of which
may have a unique physiologic effect. The primary
survey is especially important in these patients, as
even subtle findings like singed nasal hairs or facial
soot may indicate a potential for severe respiratory
compromise. Victims of fires may have burns and
require aggressive hydration and/or referral to a
burn center.

While the in-depth management of these
patients will not be discussed in detail here, it is
important to consider CO poisoning in all victims
of fires, as it may be overlooked in the dramatic presentation of a burn patient or obtunded sufferer of
smoke inhalation. Every measure must be made to
correct respiratory insufficiency that can contribute
to greater hypoxia in CO poisoning.

Cyanide Poisoning
Cyanide is produced by the combustion of carbonand nitrogen-containing compounds such as plastics,
wools, and other polymers. Cyanide binds to the
ferric ions in cytochrome c oxidase, inhibiting its action in the electron transport chain of mitochondria
and blocking aerobic respiration. The clinical features
of cyanide toxicity are similar to CO poisoning, and
CO levels have been found to correlate with cyanide
levels in victims of smoke inhalation.125 While it is
possible to measure cyanide concentrations in the
blood, the limitations in the number of laboratories
performing the assay and the time it takes to get the
results make this only useful as retrospective confirmation of the diagnosis. Therefore, the diagnosis
is clinical and its treatment empiric. Treatment of
cyanide toxicity is typically with hydroxocobalamin
(Cyanokit®) 70 mg/kg IV to a maximum of 5 g given
over 15 minutes, or a cyanide antidote kit, which is a
combination of nitrites (amyl nitrite, sodium nitrite)
followed by sodium thiosulfate 1.65 mL/kg (412
mg/kg) IV up to a 50 mL total dose.126 There are no
randomized controlled trials comparing the efficacy
of these treatments in humans.

In patients with CO poisoning and cyanide
toxicity, nitrites (which work by inducing methemoglobinemia) are contraindicated, as they further
decrease the oxygen-carrying capacity of the blood.
Thus, patients with suspected CO poisoning and
cyanide toxicity should be treated with hydroxocobalamin, when available, and/or sodium thiosulfate
without the nitrite compounds.127 As with pure CO
poisoning, HBO therapy may be beneficial in patients with concomitant CO poisoning and cyanide
toxicity, though this remains controversial.127

Chronic low-dose exposure to CO may take place
over days to years and can have wide ranging physical and mental consequences. Chronic low-level CO
exposure activates inflammatory pathways independent of COHb effects and has been associated with a
range of symptoms including: emotional and cognitive difficulties, fatigue, vertigo, paresthesia, insomnia, weakness, abdominal pain, hearing problems,
and low birth weight.54,67,128 It has been postulated
that the effects of chronic CO exposure are similar to
the pathologies in smoking. There is a constant level
of inflammation and blood viscosity is increased,129
which may account for some of these sequelae. The
incidence of chronic CO exposure is unknown and
it is likely underdiagnosed. In children, chronic CO
exposure may manifest as symptoms of memory impairment, attention-deficit/hyperactivity disorder,
poor school performance, developmental delays,
headaches, infant irritability, or nonspecific viral
symptoms.130 Without a strong clinical suspicion, a
mild elevation in laboratory COHb levels may not
be recognized as problematic.

September 2016 •

Controversies And Cutting Edge
Noninvasive Detection
Transcutaneous noninvasive pulse CO-oximeters
have been approved for clinical practice since 2005.
Standard pulse oximeters measure the absorption of
2 wavelengths of light to distinguish oxyhemoglobin from deoxyhemoglobin and cannot distinguish
between oxyhemoglobin and COHb. Pulse CO-oximetry uses at least 7 wavelengths of light to acquire
blood constituent data based on light absorption.
Some first responders and EDs have started to use
pulse CO-oximetry as a screening tool for CO poisoning. Pulse CO-oximetry may expedite the time to
diagnosis and treatment in the ED.131

Unfortunately, there are no published diagnostic
accuracy studies or subanalyses specific to pediatrics. Roth et al compared arterial to CO-oximetry
levels in 1578 patients (17 with CO poisoning) and
reported the following test characteristics using
a CO-oximetry COHb cutoff level of 6.6%: 94%
sensitivity, 77% specificity, 100% negative predictive value, and 4% positive predictive value.132 In
2013, Weaver et al published a similar study in 1363
patients with a stricter definition of CO poisoning
and found a false-positive rate of 7% when a 6% COoximetry COHb cutoff was used.133 Roth et al found
that CO-oximetry overestimates laboratory COHb
levels by about 3%; Weaver et al found it to underestimate COHb levels by 1% to 2%. The precision
has been reported as +/- 3% at 1 standard deviation.132-134 These characteristics would imply that, in
combination with symptoms and exposure, COoximetry might be helpful to screen out or confirm
15 Copyright © 2016 EB Medicine. All rights reserved.

one’s suspicion, but should not be relied on in the
absence of a confirmatory blood COHb level.

Breath CO detectors measure exhaled CO and
can be representative of a patient’s COHb level.
While these devices are validated tools for smoking
cessation in adults, there have not been any trials
looking at their use in children. In order to accurately measure CO elimination from the lungs as
opposed to inspired ambient air, breath-detector de-

vices require subjects to inhale and hold their breath
before exhaling slowly and completely. Children
may have difficulty with this technique.

Novel Treatments
Novel therapies for CO poisoning are being studied
with varying degrees of success.

In 2 prospective studies with a total of 29
patients, erythrocytapheresis (red cell exchange

Risk Management Pitfalls In The Management
Of Carbon Monoxide Exposure (Continued on page 17)
1. “I found a COHb level of 27% in my obtunded
17-year-old patient who was trying to fix a
boat motor in his garage. I am consulting the
hyperbaric medicine facility. This seemed like
a straightforward case of CO poisoning, so I
didn't consider any other testing.”
While this patient has a history and symptoms
consistent with severe CO poisoning, emergency
clinicians must always remain vigilant for cointoxicants and comorbidities. Even without
evidence of trauma on examination, a head CT
may be warranted in patients with altered mental
status, as trauma may cause or result from severe
CO poisoning. Intoxication from other drugs of
abuse can also be a precipitant to a situation of
CO poisoning. Patients with severe CO poisoning
warrant a full trauma evaluation and screening for
drugs of abuse.

4. “I have a 10-month-old boy with lethargy and
a COHb level of 22%. I remember hearing that
HBO therapy is controversial in adults and not
well studied in this population. Should I still be
consulting with a hyperbaric medicine facility?”
While there are no randomized controlled
trials for HBO in children and its use remains
controversial, the available data suggest that
it is probably safe and possibly efficacious in
preventing delayed neurologic sequelae. There
are many pediatric-specific considerations (ie,
available pediatric-trained personnel, multiplace
chambers, the need for myringotomy) in HBO
therapy, and early consultation is recommended
to ensure the proper considerations, equipment,
and personnel are in place to not delay HBO
therapy. Unstable patients should usually not
be transported, as the risks of transport often
outweigh the unclear benefit of HBO; however,
stable intubated patients may be candidates for
HBO therapy.

2. “The pulse oximeter reads 100% and the patient
does not appear cyanotic, so that means he must
not have a significant amount of COHb.”
Routine pulse oximetry cannot distinguish
between oxyhemoglobin and COHb and will
falsely read a normal oxygen saturation in cases
of CO poisoning. The machine does not reflect
the true degree of hypoxemia in CO-poisoned
patients. When available, pulse CO-oximetry
may be able to give a sense of the patient’s COHb
level. Laboratory COHb level is the only way to
confirm the presence or absence of CO poisoning.

5. “I have an adolescent patient with altered mental status and headache who endorses smoking
a waterpipe at a hookah bar but denies any
drugs other than tobacco. I have heard that
hookah smoking is clean, so it can't possibly
cause acute CO poisoning.”
Hookah (waterpipe) smoking has seen increased
popularity in the United States, with 1 in 5
adolescents endorsing smoking hookah in the
past year.142 Hookah smoking is sometimes
misunderstood as a “clean” way of smoking,
since the smoke passes through water; however,
there are many case reports and series of acute
CO poisoning from hookah smoking. A WHO
report suggested that the amount of smoke
inhalation from a 200-puff hookah smoking
session is equivalent to smoking 100 cigarettes.143

3. “I finally finished fellowship and bought a
new home for my family. Should I be installing CO detectors and how often do they need
to be checked?”
At minimum, CO detectors should be placed on
every level of the home and within 10 feet of every
bedroom door. While CO-only detectors may be
placed at any altitude in a room, combination
CO/smoke detectors should be placed on or near
the ceiling, since smoke rises. CO detectors should
be tested monthly to ensure functionality.
Copyright © 2016 EB Medicine. All rights reserved.



transfusion) has been demonstrated to reduce COHb
level and improve GCS score in conjunction with
oxygen therapy.135,136 Hyperoxygenated solution has
been found to decrease COHb levels in rats exposed
to CO poisoning and led to an improvement in cognitive test performance compared to control rats.137
Erythropoietin administration was shown in 1
randomized controlled trial of 103 patients to reduce
delayed neurologic sequelae.138

Isocapnic hyperpnea is the use of inspired gas
with 5% carbon dioxide to increase respiratory drive
and, thus, minute ventilation in a nonintubated
patient. The same strategy can be accomplished in a
ventilated patient by giving 5% carbon dioxide gas
and tailoring an increased mechanical respiratory
rate to maintain a normal blood pH. In 2 randomized
crossover trials with a total of 28 patients, isocapnic
hyperpnea has been shown to decrease COHb levels

Risk Management Pitfalls In The Management
Of Carbon Monoxide Exposure (Continued from page 16)
6. “I am seeing a 4-year-old afebrile child in the
ED with headache and malaise. A kerosene
heater was recently turned on for the winter, so
I suspected CO poisoning. The COHb level in
the child was only 4%, so this must not be the
source of his symptoms.”
Literature in children suggests that normal
levels of COHb may be ≤ 2%. In a study of
children presenting to the ED with afebrile
viral symptoms who had a potential source of
CO exposure, more than 50% of the children
had elevated (> 2%) COHb levels and all
had symptomatic improvement with oxygen
administration.49 A mild elevation in COHb may
indicate an exposure source, and a more-severe
poisoning may be prevented if it is identified
7. “The parents of a 5-year-old boy with no
significant past medical history are concerned
that something at home has been causing daily
morning headaches for the past month and a
half. They have ensured that CO detectors are
correctly installed and working, so CO poisoning must not be the etiology of his headaches.”
Normal CO detector limits are based on
preventing acute CO poisoning and will not
alarm for lower levels of exposure, which may
cause chronic CO poisoning. A COHb level in
the ED will be helpful in diagnosing this patient.
The parents should be advised that lower-limit
CO alarms are available, and it is possible to call
the fire department to have the home checked
for subalarming CO levels.
8. “While serving as medical control, I was called
by an EMS crew who were about to enter the
house of a potential CO poisoning victim.
They asked advice on initial management. I
recommended removing the victim from the
scene as quickly as possible.”
The first priority for prehospital providers treating

September 2016 •

patients with suspected CO poisoning is to ensure
scene safety. EMS personnel should not enter a
potentially dangerous situation until it has been
verified by the fire department or other agency
that it is safe to do so. There are case reports of
EMS personnel morbidity and mortality from CO
poisoning in responding to a call.
9. “I read an article about how ice resurfacers
might be a source of CO exposure. My 8-yearold hockey player presenting with headache,
nausea, and vomiting has a postgame noninvasive pulse CO-oximeter level of 6%, so this
must be CO poisoning.”
Many ice resurfacers are now electric-powered
and are not a source of CO. It would be odd
for this player to be the only victim of CO
poisoning in an arena, so other diagnoses
(concussion, dehydration, or viral illness) must
be considered. Noninvasive CO levels may
be useful for screening purposes, but, with a
precision of +/- 3% at 1 standard deviation,
must be confirmed with blood COHb levels.
NBO therapy should be given to the player
pending the confirmatory test.
10. “My 17-year-old patient has been stressed
out by school and studying too hard. She fell
asleep in her car while in the garage. Thank
goodness her mother happened to come home
early from work and found her before it was
too late. Her COHb level on presentation was
8%, it is now 2%. She was asymptomatic, so I
sent her home.”
Intentional CO poisoning is more common
and more often fatal than unintentional CO
poisoning. Comorbid mental health problems
must always be considered in victims of CO
poisoning. This patient warrants exploration
of a possible suicide attempt prior to discharge
and may require inpatient psychiatric

17 Copyright © 2016 EB Medicine. All rights reserved.

Case Conclusions

faster and increase cerebral oxygenation compared
to control NBO.139,140 With this strategy, the half-life
of CO is comparable to HBO therapy. No large trials
have been performed to demonstrate that this ventilation strategy significantly improves outcomes,
but, given the low risk, ease, and minimal expense, it
might be of benefit especially in settings where HBO
therapy is not an option.141

The 14-year-old goalie was given a normal saline 20 mL/kg
bolus for tachycardia and presumed dehydration from the
hockey game. His heart rate normalized. The patient’s disorientation resolved and his headache and nausea improved
after 2 hours of NBO therapy in the ED. In consultation
with poison control and the HBO center, the decision was
made to not transfer the patient at this time, given the rapid improvement in his symptoms. The patient was admitted
to the pediatric service and remained on 100% oxygen by
nonrebreather mask, with serial COHb levels checked every
2 hours. Eight hours after presentation, his symptoms
resolved and his COHb was 3%. He was discharged home,
and at a 6-week follow-up with his pediatrician, reported no
neurocognitive deficits.

In the hour after the first patient's arrival from the
hockey arena, many more patients arrived with symptoms
of CO poisoning. The local Poison Control Center and hyperbaric medical facility were contacted. No other victims
were as symptomatic as the goalie, who had the highest
COHb level on arrival. The source of the exposure was
found to be a faulty propane-powered ice resurfacer. The fire
department found the rink air had a CO concentration of
150 ppm.

The 2-month-old girl was placed on a 100% nonrebreather mask, which, due to hypopnea, was escalated to
noninvasive positive pressure ventilation. In consultation
with the Poison Control Center, the baby was transferred
to the nearest HBO facility. The infant had a prophylactic myringotomy to prevent middle ear rupture. She
underwent 2 90-minute dives, 12 hours apart, at 2.5 to 3
atmospheric absolute pressure. She was then transferred
back to the referring institution with a COHb of 3% and
remained on oxygen therapy for 1 more day. The baby
fed well and had normal energy prior to discharge. At
her 4-month-old follow-up appointment she had normal
growth and was learning to roll over. The source of CO
was found to be the home furnace that had a crack in the
combustion chamber resulting in a CO leak. The furnace
was positioned in the attic above the infant’s bedroom, CO
detectors had not been installed.

The 6-year-old girl was continued on 100% oxygen
through her ventilator and hydroxocobalamin was given for
empiric treatment of cyanide poisoning. She was transferred to an HBO facility and underwent 3 90-minute dives
at 2.5 atmospheric absolutes. Her hospital course was complicated by evolving acute respiratory distress syndrome
and she remained intubated and ventilated for 6 days.
Eventually, she was weaned off the ventilator and went a
home after a 14-day hospital stay. Her cyanide level from
the ED returned 2 days after presentation at 2.4 mcg/mL.
At a 3-month follow-up appointment with her pediatrician,
her mother endorses that she is having some memory difficulties and worsened school performance.

CO remains a leading cause of intentional and unintentional poisoning in the United States. While its incidence is higher during winter months and in colder
climates, there are potential sources of exposure yearround. Children may be more susceptible to CO poisoning and manifest different symptoms than adults.
In cases of mild CO poisoning, children may present
with vague symptoms of viral illness in the absence
of fever. Without a clinical suspicion, the diagnosis of
CO poisoning can be challenging. Therefore, a careful
medical and environmental history, physical examination, and appropriate utilization of noninvasive
and blood COHb levels are often needed to make the
diagnosis. NBO remains the mainstay of treatment
and should be given as soon as CO poisoning is suspected. HBO remains controversial in the treatment of
CO poisoning, though the limited research available
suggests it is safe in children and consultation with a
hyperbaric medicine center is warranted in cases of
moderate and severe CO poisoning.

Time- And Cost-Effective Strategies
• Noninvasive CO detection with pulse COoximetry may decrease the time to diagnosis of
CO poisoning and to referral to an HBO facility,
though its cost effectiveness has yet to be studied.
In a study by Hampson, patients screened with
pulse CO-oximetry were referred to an HBO facility 1 hour sooner than those not screened with
pulse CO-oximetry, which may save personnel
time and resources in the referring ED.131
Risk management caveat: All COHb levels obtained from noninvasive pulse CO-oximeters
must be confirmed with a laboratory blood
sample, as the precision of these devices is
+/- 3% at 1 standard deviation, varies in patient
populations, and is not validated in children.
• Oxygen should be applied immediately in all
cases of suspected CO poisoning even before
having a definitive COHb level. As oxygen is
inexpensive, generally harmless, and the mainstay of treatment, providing oxygen early will
decrease a patient’s length of stay, improve
symptoms sooner, and possibly avoid an inpatient admission for continued therapy.

Copyright © 2016 EB Medicine. All rights reserved.



Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are
equally robust. The findings of a large, prospective,
randomized, and blinded trial should carry more
weight than a case report.

To help the reader judge the strength of each
reference, pertinent information about the study, such
as the type of study and the number of patients in the
study is included in bold type following the references,
where available. The most informative references cited
in this paper, as determined by the authors, are noted
by an asterisk (*) next to the number of the reference.

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September 2016 •

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September 2016 •

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1. Which of the following is NOT a source of
a. An electric-powered space heater
b. A charcoal barbecue grill
c. A propane-powered ice resurfacer
d. A gasoline-powered portable electric
2. Which of the following best estimates the halflife of COHb with 100% oxygen therapy by
nonrebreather face mask?
a. 20 minutes
b. 60 minutes
c. 3 hours
d. 6 hours
3. Which of the following statements regarding
home CO alarms is FALSE?
a. CO-only detectors can be placed at any
altitude in a room.
b. CO alarms will immediately alert when
the air CO concentration exceeds a certain
c. CO alarms may not detect chronic CO
d. CO alarms should be placed on every level
of a home and near every bedroom door.
4. What is the first priority for prehospital providers when responding to a call of suspected
CO poisoning?
a. Apply oxygen.
b. Ensure scene safety.
c. Remove the patient from the source of
d. Conduct a primary survey.

September 2016 •

5. Which of the following statements regarding
delayed neurologic sequelae is TRUE?
a. A head CT is useful in predicting delayed
neurologic sequelae.
b. Evidence suggests delayed neurologic
sequelae are more common in adults than
c. Risk of delayed neurologic sequelae is
closely related to the COHb level on ED
d. Delayed neurologic sequelae are always
6. What is the upper limit of normal COHb in
nonsmoking children?
a. 0%
b. 2%
c. 5%
d. 10%
7. Which of the following statements regarding
intentional CO poisoning is FALSE?
a. Co-intoxicants are rarely present.
b. The death rate is higher than in
unintentional CO poisoning.
c. Psychiatric assessment is warranted prior to
d. The most common source is motor vehicle
8. What is the mainstay for treatment of CO poisoning?
a. Erythropoietin
b. Oxygen
c. Exchange transfusion
d. Hyperventilation
9. Which of the following cyanide treatments is
contraindicated in CO poisoning?
a. Hydroxocobalamin
b. Sodium thiosulfate
c. Hyperbaric oxygen therapy
d. Sodium nitrite
10. Which of the following statements regarding
noninvasive detection of COHb is TRUE?
a. Pulse CO-oximetry has been validated in
b. Breath CO testing has been validated in
c. The reported precision of pulse COoximeters is about 3%.
d. CO poisoning is not present in patients with
normal oxygen saturations.

The authors would like to thank Alison Clapp MLIS
for her assistance with the literature review and Dr.
Matthew Eisenberg for providing feedback on the
23 Copyright © 2016 EB Medicine. All rights reserved.



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Termination date: September 1, 2019.
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